Journal
ISCIENCE
Volume 23, Issue 10, Pages -Publisher
CELL PRESS
DOI: 10.1016/j.isci.2020.101602
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Funding
- European Research Council (ERC) under the European Union [694354]
- Austrian Science Fund [P31773]
- European Research Council (ERC) [694354] Funding Source: European Research Council (ERC)
- Austrian Science Fund (FWF) [P31773] Funding Source: Austrian Science Fund (FWF)
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CDK6 is frequently overexpressed in various cancer types and functions as a positive regulator of the cell cycle and as a coregulator of gene transcription. We provide evidence that CDK6 is involved in the process of DNA methylation, at least in ALL. We observe a positive correlation of CDK6 and DNMT expression in a large number of ALL samples. ChIP-seq analysis reveals CDK6 binding to genomic regions associated with DNA methyltransferases (DNMTs). ATAC-seq shows a strong reduction in chromatin accessibility for DNMT3B in CDK6-deficient BCR-ABL(+) Cdk6(-/-) cells, accompanied by lower levels of DNMT3B mRNA and less chromatin-bound DNMT3B, as shown by RNA-seq and chromatome analysis. Motif analysis suggests that ETS family members interact with CDK6 to regulate DNMT3B. Reduced representation bisulfite sequencing analysis uncovers reversible and cell line-specific changes in DNA methylation patterns upon CDK6 loss. The results reveal a function of CDK6 as a regulator of DNA methylation in transformed cells.
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